The changing pattern and implications of multiple organ failure after blunt injury with hemorrhagic shock

University of Texas Southwestern Medical Center and Parkland Health and Hospital System, Dallas, TX, USA.
Critical care medicine (Impact Factor: 6.31). 10/2011; 40(4):1129-35. DOI: 10.1097/CCM.0b013e3182376e9f
Source: PubMed


To describe the incidence of postinjury multiple organ failure and its relationship to nosocomial infection and mortality in trauma centers using evidence-based standard operating procedures.
Prospective cohort study wherein standard operating procedures were developed and implemented to optimize postinjury care.
Seven U.S. level I trauma centers.
Severely injured patients (older than age 16 yrs) with a blunt mechanism, systolic hypotension (<90 mm Hg), and/or base deficit (≥6 mEq/L), need for blood transfusion within the first 12 hrs, and an abbreviated injury score ≥2 excluding brain injury were eligible for inclusion.
One thousand two patients were enrolled and 916 met inclusion criteria. Daily markers of organ dysfunction were prospectively recorded for all patients while receiving intensive care. Overall, 29% of patients had multiple organ failure develop. Development of multiple organ failure was early (median time, 2 days), short-lived, and predicted an increased incidence of nosocomial infection, whereas persistence of multiple organ failure predicted mortality. However, surprisingly, nosocomial infection did not increase subsequent multiple organ failure and there was no evidence of a "second-hit"-induced late-onset multiple organ failure.
Multiple organ failure remains common after severe injury. Contrary to current paradigms, the onset is only early, and not bimodal, nor is it associated with a "second-hit"-induced late onset. Multiple organ failure is associated with subsequent nosocomial infection and increased mortality. Standard operating procedure-driven interventions may be associated with a decrease in late multiple organ failure and morbidity.

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Available from: Ernest E Moore, Oct 04, 2015
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    • "Preferably the presence of preoperative organ dysfunctions should be included in the final complication grade as an addendum indicating that the patient had organ dysfunction before surgery. Because peritonitis [10] or severe bleeding due to trauma [11] may cause organ dysfunctions, all postoperative organ dysfunctions should not be classified as surgical complications. In this study postoperative organ dysfunctions were not classified as complications if it they were already present preoperatively i.e. the patient’s condition remained unchanged in terms of organ dysfunctions. "
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    ABSTRACT: Background Patients undergoing emergency surgery have a high risk for surgical complications and death. The Clavien-Dindo classification has been developed and validated in elective general surgical patients, but has not been validated in emergency surgical patients. The aim of the current study was to evaluate the Clavien-Dindo classification of surgical complications in emergency surgical patients and to study preoperative factors for risk stratification that should be included into a database of surgical complications. Methods A cohort of 444 consecutive patients having emergency general surgery during a three-month period was retrospectively analyzed. Surgical complications were classified according to the Clavien-Dindo classification. Preoperative risk factors for complications were studied using logistic regression analysis. Results Preoperatively 37 (8.3%) patients had organ dysfunctions. Emergency surgical patients required a new definition for Grade IV complications (organ dysfunctions). Only new onset organ dysfunctions or complications that significantly contributed to worsening of pre-operative organ dysfunctions were classified as grade IV complications. Postoperative complications developed in 115 (25.9%) patients, and 14 (3.2%) patients developed grade IV complication. Charlson comorbidity index, preoperative organ dysfunction and the type of surgery predicted postoperative complications. Conclusions The Clavien-Dindo classification of surgical complications can be used in emergency surgical patients but preoperative organ dysfunctions should be taken into account when defining postoperative grade IV complications. For risk stratification patients’ comorbidities, preoperative organ dysfunctions and the type of surgery should be taken into consideration.
    Patient Safety in Surgery 07/2014; 8(1):31. DOI:10.1186/1754-9493-8-31
  • Critical care medicine 04/2012; 40(4):1348-9. DOI:10.1097/CCM.0b013e31823e9501 · 6.31 Impact Factor
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    ABSTRACT: Although melatonin treatment following trauma-hemorrhage or ischemic reperfusion prevents organs from dysfunction and injury, the precise mechanism remains unknown. This study tested whether melatonin prevents liver injury following trauma-hemorrhage involved the protein kinase B (Akt)-dependent heme oxygenase (HO)-1 pathway. After a 5-cm midline laparotomy, male rats underwent hemorrhagic shock (mean blood pressure approximately 40 mmHg for 90 min) followed by fluid resuscitation. At the onset of resuscitation, rats were treated with vehicle, melatonin (2 mg/kg), or melatonin plus phosphoinositide 3-kinase (PI3K) inhibitor wortmannin (1 mg/kg). At 2 hr after trauma-hemorrhage, the liver tissue myeloperoxidase activity, malondialdehyde, adenosine triphosphate, serum alanine aminotransferase, and aspartate aminotransferase levels were significantly increased compared with sham-operated control. Trauma-hemorrhage resulted in a significant decrease in the Akt activation in comparison with the shams (relative density, 0.526 ± 0.031 versus 1.012 ± 0.066). Administration of melatonin following trauma-hemorrhage normalized liver Akt phosphorylation (0.993 ± 0.061), further increased mammalian target of rapamycin (mTOR) activation (5.263 ± 0.338 versus 2.556 ± 0.225) and HO-1 expression (5.285 ± 0.325 versus 2.546 ± 0.262), and reduced cleaved caspase-3 levels (2.155 ± 0.297 versus 5.166 ± 0.309). Coadministration of wortmannin abolished the melatonin-mediated attenuation of the shock-induced liver injury markers. Our results collectively suggest that melatonin prevents hemorrhagic shock-induced liver injury in rats through an Akt-dependent HO-1 pathway.
    Journal of Pineal Research 05/2012; 53(4):410-6. DOI:10.1111/j.1600-079X.2012.01011.x · 9.60 Impact Factor
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